Actions of adenosine on normal and abnormal impulse initiation in canine ventricle.

We studied the role of adenosine in modulating pacemaker activity in normal and infarcted ventricular tissues. We used standard microelectrode techniques to study the effects of adenosine on impulse initiation in Tyrode's superfused normal canine Purkinje fibers (PF), PF obtained from experimentally infarcted hearts, and BaCl2-superfused PF. Adenosine reduced automaticity of normal PF, whereas beta, gamma-methylene ATP did not. In infarcted and in Ba2+-depolarized PF, adenosine had no effect on automaticity or the action potential. We then used intracellular current injection to vary the membrane potentials of normal PF and found adenosine to depress automaticity more at high than at low membrane potentials. The ability of adenosine to counteract the effects of epinephrine on automaticity also was related to membrane potential. We conclude that adenosine depresses normal automaticity but has little effect on abnormal impulse initiation at low membrane potentials. It therefore appears that in the setting of myocardial infarction or ischemia the extent to which adenosine release will modify the function of normal and ectopic pacemakers will be influenced by the membrane potentials of those pacemakers.